Figure 3: Classification of Neuropathic Pain
Note : Finnerup, N. B., Kuner, R., & Jensen, T. S. (2021). Neuropathic pain: From mechanisms to treatment. Physiological Reviews, 101(1), 259–301. Recreated by permission from the Journal of Physiological Reviews free reuse. Copyright policy as listed at https://journals.physiology.org/publication-process#copyright.
Disease-based classification of neuropathic pain Different pain studies have generally classified neuropathic pain based on the related underlying disease. Regarding the newly released ICD11 classification, neuropathic pain is first organized into peripheral and central neuropathic pain based on the location of the lesion or disease in the Trigeminal neuralgia This term describes a specific type of orofacial pain affecting one or more divisions of the trigeminal nerve. The diagnosis depends on the patient’s description of characteristic electric shock-like pain attacks that are abrupt in onset and termination, last a few seconds to less than 2 minutes, and occur spontaneously or evoked by innocuous stimuli at trigger zones. The trigger zones are within cutaneous or mucous trigeminal areas, and chewing, touching, tooth brushing, or washing may provoke a paroxysm. It is debated whether the spontaneous attacks are truly spontaneous or stimulus-depended attacks triggered by subclinical stimuli. The frequency of attacks varies. There is often a remission period lasting weeks to years when patients are pain-free. Despite being classified as a peripheral neuropathic pain, the lesion is often within the root entry zone, where the myelin is primarily produced by central nervous system oligodendrocytes that extend beyond the pons and transit into myelin produced by peripheral Schwann cells, and the lesion may also be in the brain stem within the central nervous system, and trigeminal neuralgia is thus sometimes a central pain condition (Chen et al., 2022). The principal underlying cause of classical trigeminal neuralgia is considered to be a vascular compression of the trigeminal nerve root in the cisternal segment, the root entry zone, or the pontine segment resulting in morphological changes and atrophy in the nerve. There is also evidence suggesting that the effect of microsurgical decompression or radiosurgery is related to more severe compression of the nerve. Electron-microscopic and immunohistochemical
peripheral or central somatosensory nervous system. Within each of these categories, pain is classified into different neuropathic pain conditions based on the underlying disease.
examinations of nerve biopsies taken during surgery for microvascular decompression have shown demyelination and myelin abnormalities as well as axonal damage, atrophy, and sprouting. The prevailing theory is that spontaneous pain paroxysms are generated by spontaneous discharges in damaged neurons with a lowered threshold for repetitive firing and cross-excitation to hyperexcitable neighboring neurons. Since there may be an immediate relief of microvascular decompression and recovery of trigeminal nerve root conduction, it is suggested that the underlying cause can be a transient conduction nerve block. Functional cross-excitation between neurons may also explain pain evoked by touching trigger zones with spike activity in large, myelinated A fibers activated by touch, causing depolarization in neighboring C-neurons. Progression to severe nerve root damage is likely to cause more prominent sensory loss and possible continuous pain because of continuous ectopic discharges. Retrograde biochemical disturbances and the immune reaction of the trigeminal ganglion and inflammation may also be involved. Neuroimaging studies have also documented subtle gray and white matter loss in brain areas involved in pain perception, but it is unclear if these changes are secondary and adaptive changes to ongoing activity from focal nerve damage or if they contribute to pain (Xia et al., 2022). The unique acute response of this neuropathic pain condition to microvascular decompression, radiofrequency ablation, and other treatments targeting the nerve directly supports that the pain generator is within the damaged section of
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